Abstract
Multiple sclerosis (MS) is an inflammatory autoimmune demyelinating disease of the central nervous system (CNS) [1]. Its debilitating effects on sensory, motor, autonomic, and neurocognitive functions affect primarily young adults, especially women (two to three times more frequent than in men), and is most frequent in northern countries, affecting more than 150 individuals of every 100,000 inhabitants e.g. in Canada and the Scandinavian countries. The development of this often initially relapsing/remitting and later progressive disease is associated with genetic and environmental risk factors [1, 3]. The major histocompatibility complex (MHC) class II gene locus is by far the most prominent genetic risk factor, and altered immune responses to the Epstein Barr virus (EBV), the causative infectious agent of most cases of infectious mononucleosis or "kissing disease", have in recent years emerged as the most prominent environment induced risk factors for MS [1]. Interestingly, particularly infectious mononucleosis as symptomatic primary EBV infection, caused by a lymphocytosis of mainly lytic EBV antigen specific CD8(+) T cells, and elevated antibody responses against EBV have been found to synergize with the MS associated MHC class II molecule HLA-DRB1*1501 to increase MS risk seven- to fifteen-fold, respectively [1]. Moreover, EBV infection seems to precede MS onset by several years in nearly all patients. Thus, EBV infection currently appears as a prerequisite for MS development that increases the risk for this autoimmune disease in genetically susceptible individuals.